Abstract

Lipopolysaccharide (LPS) derived from a parental strain, Salmonella typhimurium ES878, was more toxic for mice than LPS derived from two rough variants, S. typhimurium ES878R and S. typhimurium ES878SIII. The interaction of any of the three LPS with isolated rat-liver mitochondria (RLM) and rat-heart mitochondria (RHM) resulted in a loss of respiratory control and in the inhibition of the state 3 respiration rate. These effects were only observed if LPS was added to the mitochondrial suspension before addition of substrate. RHM treated with LPS assumed the nonenergized orthodox mode of the cristae when LPS was added to RHM prior to substrate. The ability of LPS to remove respiratory control of isolated RLM and RHM could be used more efficiently to quantitate the relative toxicities of the LPS than could determinations of LD50 for mice. When the mitochondrial assay system was used, the rough variant LPS proved to be more toxic than LPS derived from the parental strain, S. typhimurium ES878.

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